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Translational Research in Cancer Drug Development Meiyanto, Edy; Hermawan, Adam; Anindyajati, .
Indonesian Journal of Cancer Chemoprevention Vol 2, No 2 (2011)
Publisher : Indonesian Research Gateway

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (4.399 KB)

Abstract

The development of cancer treatment were initiated by the existence of human’s effort to treat by applying certain materials which is mostly part(s) or extracts of plants, which are now adapted as traditional herbal medicine. The discovery of new drugs was based on intuition and empirical evidence. Thus, high luck factor was involved in a successful treatment with unguaranteed reproducibility. One example of drug being developed through conventional drug development is Taxol. Taxol is an extremely complex natural product and requires a bunch of hard work with high level of serendipity to be discovered as antitumor agent. Recently, rapid development in human biology and technology allow a change in drug discovery strategy by minimizing the luck factor. Targeted therapy has been a very promising strategy of drug development research, especially in cancer treatment. Although cancer has been known as a disease with very complex cellular and histo-pathophysiology, the abundance of studies on proteins, such as receptors and hormones, as the hallmarks of cancer allows us to explore carcinogenesis suppression further based on molecular targeted therapy. Kinases, one type of protein involved in signal transduction regulating cell growth and differentiation, could be the proteins that  are proposed to be inhibited in suppressing tumor growth. An interesting example of the drug being discovered based on molecular modeling is the discovery of lapatinib as anti-cancer with specific target on HER-2 and EGFR to overcome the resistance of cancer  to Herceptin caused by elevated level of EGFR expression.
POTENSI EKSTRAK ETANOLIK KULIT BUAH JERUK NIPIS (Citrus aurantiifolia (Cristm.) Swingle) SEBAGAI AGEN KHEMOPREVENTIF MELALUI PENEKANAN EKSPRESI c-Myc DAN PENGHAMBATAN PROLIFERASI PADA SEL PAYUDARA TIKUS GALUR SPRAGUE DAWLEY TERINDUKSI 7,12-DIMETILBENZ[a]ANTRASENA Meiyanto, Edy; Pratiwi, Dewi; Hastuti, Novi; Nur W, Niken; Armandari, Inna; Ikawati, Muthi’; Hermawan, Adam
Majalah Obat Tradisional Vol 15, No 1 (2010)
Publisher : Faculty of Pharmacy, Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (702.754 KB) | DOI: 10.14499/mot-TradMedJ15iss1pp%p

Abstract

POTENSI  EKSTRAK ETANOLIK KULIT BUAH JERUK NIPIS (Citrus aurantiifolia (Cristm.) Swingle) SEBAGAI AGEN KHEMOPREVENTIF MELALUI PENEKANAN EKSPRESI c-Myc DAN PENGHAMBATAN PROLIFERASI PADA SEL PAYUDARA TIKUS GALUR SPRAGUE DAWLEY TERINDUKSI 7,12-DIMETILBENZ[a]ANTRASENA POTENCY OF CITRUS PEELS (Citrus aurantiifolia (Cristm.) Swingle) ETHANOLIC EXTRACT AS CHEMOPREVENTIVE  AGENT THROUGH DOWNREGULATION OF           c-Myc EXPRESSION AND INHIBITION OF 7.12-DIMETHYLBENZ[a]ANTRACHENE INDUCED FEMALE  SPRAGUE DAWLEY RATS BREAST CELL PROLIFERATION Dewi Pratiwi, Novi Hastuti, Niken Nur W, Inna Armandari, Muthi’ Ikawati,Adam Hermawan  dan Edy Meiyanto*)Cancer Chemoprevention Research Center Fakultas Farmasi, Universitas Gadjah Mada ABSTRAK Penggunaan obat berbasis alam saat ini berkembang pesat di semua kalangan masyarakat. Selain karena harga yang lebih terjangkau, obat berbasis alam relatif lebih aman dibandingkan dengan obat sintetik. Kulit jeruk nipis (Citrus aurantiifolia) merupakan salah satu obat berbasis alam mengandung flavonoid yang berpotensi sebagai antikarsinogenesis.  Penelitian ini dirancang untuk mengkaji potensi kulit jeruk nipis (C. aurantiifolia) dalam menekan proliferasi sel  payudara tikus galur Sprague Dawley yang terinduksi 7,12-Dimetilbenz[a]Antrasena (DMBA).  Dalam penelitian ini, tikus dibagi menjadi lima kelompok yakni kelompok perlakuan DMBA, kelompok perlakuan CMC-Na, kelompok perlakuan ekstrak dosis 1500 mg/kgBB , kelompok perlakuan DMBA+ekstrak dosis 750 mg/kgBB dan perlakuan DMBA+ekstrak dosis 1500 mg/kgBB. Pengamatan proliferasi sel payudara dengan metode AgNOR menunjukkan bahwa pemberian ekstrak kulit C. aurantiifolia dapat menekan proliferasi sel secara signifikan. Secara kuantitatif signifikansi yang dihasilkan dosis  1500 mg/kgBB lebih tinggi daripada dosis 750 mg/kgBB. Hasil pengamatan imunohistokimia pada ekspresi c-Myc mendukung data sebelumnya. Pada kelompok dosis 750 terlihat warna coklat pada sitosol yang lebih intens dibanding kelompok dosis 1500. Ekstrak etanolik kulit jeruk nipis dapat menekan proliferasi sel payudara terinduksi DMBA, penekanan proliferasi tersebut meningkat seiring peningkatan dosis sehingga jeruk nipis dapat digunakan sebagai agen khemopreventif.
Aktivitas Antiproliferasi Ekstrak Etanolik Herba Ciplukan (Physalis angulata L.) Terhadap Sel Hepar Tikus Betina Galur Sprague Dawley Terinduksi 7,12-Dimetilbenz[a]antrasena Agusta Fauzi, Ilham; Amalia, Fikri; Sabila, Nurma; Hermawan, Adam; Ikawati, Muthi; Meiyanto, Edy
Majalah Kesehatan Pharmamedika Vol 3, No 1 (2011): JANUARI - JUNI 2011
Publisher : Lembaga Penelitian Universitas YARSI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33476/mkp.v3i1.434

Abstract

One of the natural materials as potentially efficacious chemopreventive agents are Ciplukan (Physalis angulata L.). Several previous studies reported that Physalis angulata L. herbs ethanolic extract (PEE) has cytotoxic activity and induction of apoptosis in breast cancer cells MCF-7 and HeLa cervical cancer cells. This study aims to determine the effects of  PEE as an chemopreventive agent on rat liver cells induced 7,12-dimetilbenz[a]anthracene (DMBA). This study used Sprague Dawley strain female rats aged 40-50 days were divided into 5 groups : (1) DMBA control group, mice were induced with DMBA in per oral dose of 20 mg/kg; (2) DMBA + PEE dose 750 mg/kgBW group ; (3) DMBA + PEE dose 1500 mg/kgBW group ; (4) solvent control group of CMC-Na 0,5%; (5) PEE dose 1500 mg/kgBW control group. PEE was dissolved in CMC-Na 0,5% and administered daily, starting the seventh week after administration of DMBA. At the beginning of  the tenth week of the study, rats were necropted and liver organs were isolated and stored in buffered formalin 4%. Qualitative analysis to determine the histopathology of liver cells through staining method of Hematoxyllin Eosin (HE), while quantitative analysis to determine the level of liver cell proliferation by AgNOR staining method. The results showed in the DMBA control group that liver cell morphology changes that hiperproliferation leading to carcinogenesis. In DMBA + PEE dose of  1500 mg/kgBW group improved the situation of DMBA-induced liver cells histopathology and antiproliferation activity better than DMBA + PEE dose of 750 mg/kgBW on DMBA-induced rat liver cells. The results showed that Physalis angulata L. herbs ethanolic extract can inhibit cell proliferation in rat liver caused by DMBA administration through antiproliferation mechanism and have potential for the development as chemoprevention material on liver cancer
AKTIVITAS SITOTOKSIK EKSTRAK ETANOLIK HERBA CIPLUKAN (Physalis angulata L.) PADA SEL KANKER LEHER RAHIM HeLa MELALUI MODULASI EKSPRESI PROTEIN p53 Darma, Andita Pra; Ashari, Rosana Anna; Nugroho, Perdana Adhi; Monikawati, Ameilinda; Fauzi, Ilham Agusta; Hermawan, Adam; Meiyanto, Edy
Farmasains : Jurnal Farmasi dan Ilmu Kesehatan Vol 1, No 2 (2011): Oktober 2010 - Maret 2011
Publisher : University of Muhammadiyah Malang

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1280.681 KB) | DOI: 10.22219/far.v1i2.1163

Abstract

Cervical cancer is one of leading cause of cancer death in women in the developing countries. One of the strategy to prevent cervical cancer based on cytotoxic agents are now being developed. Ciplukan (Physalis angulata L.) is one of potential plant as chemopreventive agent due to Physalin and Withangulatin constituent in this plant. This study was aimed to know cytotoxic effect  of ciplukan ethanolic extract (CEE) in human cervical carcinoma Hela cell line. Evaluation of cell viability value was determined using MTT assay. The expression of p53 as cell proliferation regulator was observed with immunocytochemistry assay. Ethanolic extract of ciplukan showed cytotoxic effect in HeLa cell line with IC50 of 158 µg/ml. Further observation of cell proliferation regulator showed that CEE induces expression of p53 that inhibit cell proliferation. The result showed that CEE has potential activity to be developed as anticancer agent in human cervical cancer.
Usulan Strategi Komunikasi Pemasaran Untuk Perusahaan Teknologi (Studi pada: UX Custom) Hermawan, Adam
Strategic : Jurnal Pendidikan Manajemen Bisnis Vol 20, No 2 (2020): Strategic
Publisher : Universitas Pendidikan Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.17509/strategic.v20i2.28216

Abstract

DAFTAR PUSTAKAAbdurrahman, M. S. (2017, May 20). tekno.liputan6.com. (Liputan 6) Retrieved August 3, 2017, from http://tekno.liputan6.com/http://tekno.liputan6.com/read/2957050/pertumbuhan-e-commerce-indonesia-tertinggi-di-duniaArmstrong, G., Kotler, P. (2005). Principle of Marketing (Fourth ed.). New Jersey: Pearson Prentice-Hall.Armstrong, G., Kotler, P. (2009). An Introduction Marketing (Ninth ed.). (Pearson, Ed.) Prentice Hall.Das, K., Gryseels , M., Sudhir, P., Tan , K. T. (2016). Unlocking Indonesia’s digital opportunity. McKinsey Indonesia Office.Golafshani, N. (2003). Understanding Reliability and Validity in Qualitative Research. The Qualitative Report, 8.Grover, R., Vriens, M. (2006). The Handbook of Marketing Research: Uses, Misuses, and Future Advances. United States of America: SAGE .Keller, K. L. (2008). Strategic Brand Management, (Third ed.). Upper Saddle River, New Jersey: Pearson Prentice-Hall.KEMP, S. (2017, April 26). wearesocial.com. Retrieved from https://wearesocial.com/special-reports/state-internet-q2-2017Kotler, P., Keller, K. L. (2009). Manajemen Pemasaran (Thirteenth ed.). (A. Maulana, Y. S. Hayati, Eds., B. Sabran, Trans.) Pearson Education Penerbit Erlangga.Kumar, G. S. ( 2007). Handbook Of Management Terms. ICFAI .Patton, M. Q. (2001). Qualitative Research Evaluation Methods.Porter, M. E. (2008). The Five Competitive Forces That Shape Strategy. Harvard Business Review.Pratama, A. H. (2017, January 30). id.techinasia.com. Retrieved from techinasia.com: https://id.techinasia.com/pertumbuhan-pengguna-internet-di-indonesia-tahun-2016Purba, H.H. 2008, September 25.       DiagramFishbone dari Ishikawa, Kaoru. Teknik Penuntun Pengendalian Mutu, Penerbit Mediyatama Sarana PerkasaRosen, D. E., Elizabeth Purinton. (2004). Website design: Viewing the web as a cognitive landscape. Journal of Business Research, 57.Rumahweb. (2007, October 1). Retrieved from Rumahweb.com: https://www.rumahweb.com/journal/web-developer-web-designer-dan-webmaster.htmWilson, P. F., Dell, L. D., Anderson, G. F. (1993). Root Cause Analysis : A Tool for Total Quality Management (First ed.). American Society for Quality.
Hesperidin increase cytotoxic effect of doxorubicin in MCF-7 cells Hermawan, Adam; Meiyanto, Edy; Susidarti, Ratna Asmah
Indonesian Journal of Pharmacy Vol 21 No 1, 2010
Publisher : Faculty of Pharmacy Universitas Gadjah Mada, Yogyakarta, Skip Utara, 55281, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (514.522 KB) | DOI: 10.14499/indonesianjpharm0iss0pp8-17

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Hesperidin,  a  flavonoid,  shows  strong  cytotoxic  effect  in  several  cancer cell  lines.  The  aim  of  this  research  was  to  investigate  cytotoxic  activities  of hesperidin  alone  and  in  combination  with  doxorubicin.  Cell  viability  assay  of hesperidin,  doxorubicin,  and  combination  treatments  were  carried  out  by  using MTT  assay.  Apoptosis  assay  was  done  using  double  staining  method  using Ethidium  Bromide-Acridine  Orange.  Hesperidin  did  not  show  cytotoxic  effect but doxorubicin showed cytotoxic effect with IC50467 nM. Hesperidin (5, 50 and 100  µM)  increased  cytotoxic  effect  of  doxorubicin  compared  with  doxorubicin alone.  The  strongest  cytotoxic  activity  was  showed  by  the  combination  of  200 nM  doxorubicin  and  100  µM  hesperidin.  Combination  treatment  of  doxorubicin 200  nM  and  hesperidin  100  µM  induced  apoptosis  in  MCF-7 cells.  Hesperidin  is potentially  to  be  developed  as  co-chemotherapeutic  agent  for  breast  cancer, while molecular mechanism need to be explored.Key words: Hesperidin, doxorubicin, synergism, MCF-7, apoptosis 
Data mining analysis of miR-638 and key genes interaction in cisplatin resistant triple-negative breast cancer Adam Hermawan; Herwandhani Putri
Indonesian Journal of Biotechnology Vol 24, No 2 (2019)
Publisher : Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (335.426 KB) | DOI: 10.22146/ijbiotech.48732

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Cisplatn is one of the chemotherapy for the treatment of triple‐negatve breast cancer (TNBC), but its effectveness is limited because of the phenomenon of chemoresistance. miR‐638 was shown to regulate chemoresistance; however, it has never been validated in the cisplatn‐resistant tumor from patents. This present study aimed to identfy the key gene regulatory networks of miR‐638 and evaluate the potental role of the miR‐638 and its targets as potental prognosis biomarkers for cisplatn‐resistance triple‐negatve breast cancer patents. The miR‐638 target was obtained from the miRecords database while the mRNA of chemoresistance biomarker candidate was obtained from the GSE18864 of GEO database, which is mRNA of cisplatn‐resistance TNBC patents. CCND1 and FZD7 are potental candidates for cisplatn chemoresistance biomarkers in patents with TNBC. Moreover, a Kaplan‐Meier survival plot showed that breast cancer patents with low mRNA levels of FZD7 had signifcantly worse overall survival than those in higher mRNA expression group. Taken together, miR‐638 plays a role in cisplatn resistance mechanism through a mechanism involving its target gene CCND1 and FZD7. Overall, miR‐638, CCND1, and FZD7 are candidates for cisplatn biomarker resistance in TNBC.
Ethanolic extract of sappan wood (Caesalpinia sappan L.) inhibits MCF-7 and MCF-7/HER2 mammospheres' formation: an in vitro and bioinformatic study Dhania Novitasari; Laeli Muntafiah; Nur Fitra Sari; Edy Meiyanto; Adam Hermawan
Indonesian Journal of Biotechnology Vol 26, No 3 (2021)
Publisher : Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.22146/ijbiotech.63510

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One of the mechanisms of cancer cell resistance toward chemotherapy is through cancer stem cells (CSCs), which are characterized by excessive activation of regulator proteins such as human epidermal receptor 2 (HER2). Sappan wood (Caesalpinia sappan L.) contains brazilin and brazilein that exhibit cytotoxic effects on several cancer cell lines. We aimed to explore the potency of the ethanolic extract of sappan (EES) in CSCs through bioinformatic analyses and by using a three-dimensional (3D) breast cancer stem cells (BCSCs) for in vitro assay with two different models (i.e., BCSCs and HER2-BCSCs) in order to identify the potential therapeutic targets of genes (PTTGs). Bioinformatic analyses identified PTTGs, which were further analyzed by gene ontology, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, protein-protein interaction (PPI) networks, and hub protein selection. Mammospheres were cultured under conditioned media. The cytotoxic effects of EES were then measured by direct counting and based on the mammosphere-forming potential (MFP). Bioinformatic analysis disclosed PIK3CA and TP53 as PTTGs in BCSCs and HER2-BCSCs, respectively. In addition, the KEGG pathway analyses also demonstrated that PTTGs could regulate the ERBB pathway. EES thus demonstrated cytotoxicity and inhibited the formation of mammospheres. Collectively, EES exhibited excellent potential for further development as an inhibitor of cancer stem cells in breast cancer.
POTENSI EKSTRAK ETANOLIK KULIT BUAH JERUK NIPIS (Citrus aurantiifolia (Cristm.) Swingle) SEBAGAI AGEN KHEMOPREVENTIF MELALUI PENEKANAN EKSPRESI c-Myc DAN PENGHAMBATAN PROLIFERASI PADA SEL PAYUDARA TIKUS GALUR SPRAGUE DAWLEY TERINDUKSI 7,12-DIMETILBENZ[a]ANTRASENA Dewi Pratiwi; Novi Hastuti; Niken Nur W; Inna Armandari; Muthi’ Ikawati; Adam Hermawan; Edy Meiyanto
Majalah Obat Tradisional Vol 15, No 1 (2010)
Publisher : Faculty of Pharmacy, Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (702.754 KB) | DOI: 10.22146/tradmedj.8063

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The using of natural-based medicine is growing rapidly in societies. Besides being cheap and affordable, natural-based medicine is relatively safer than the synthetic drugs. Peel of Citrus aurantifolia (Cristm.) Swingle) is one of the chemopreventive agent which contain flavonoids have potency as anticarcinogenic agent. This study is designed to study the potency of Citrus aurantifolia peel ethanolic extract in proliferation inhibition of Rattus norvegicus mammary cell of Sprague Dawley strain which is induced by 7,12-Dimethylbenz[a]anthracene (DMBA). Rats were divided into five groups consist of DMBA treatment, CMC-Na treatment, extract 1500 mg/kgBW treatment, treatment of DMBA+ extract 750 mg/kgBW and DMBA+ extract 1500 mg/kgBW. At the beginning of the tenth week of the study, breasts was isolated and stored in 10% formalin buffer. Observation of cell proliferation was done by AgNOR method. C-Myc expression observed using immunohistochemistry (IHC). Observation of mammary cell with AgNOR method indicated that the treatment of Citrus aurantifolia peel ethanolic extract can inhibit cell proliferation significantly. Dosage 1500 mg/kgBW gave higher inhibition effect than dosage 750 mg/kgBW. IHC result showed that treatment of Citrus aurantifolia peel ethanolic extract decrease the expression of c-Myc. Dosage 750 mg/kgBW gave lower decreasing effect than dosage 1500 mg/kgBW. Citrus aurantifolia peel ethanolic extract inhibited the proliferation of mammary cell induced DMBA through the inhibition of c-Myc expression in dose dependent phenomena so that it is a potential chemopreventive agent.
Curcumin Analogs Induce Apoptosis and G2/M Arrest In 4T1 Murine Triple-Negative Breast Cancer Cells Retno Murwanti; Azmi Rahmadani; Ritmaleni Ritmaleni; Adam Hermawan; Bambang Sulistiyo Ari Sudarmanto
Indonesian Journal of Pharmacy Vol 31 No 1, 2020
Publisher : Faculty of Pharmacy Universitas Gadjah Mada, Yogyakarta, Skip Utara, 55281, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.14499/indonesianjpharm31iss1pp11

Abstract

Chemotherapy is the first-line treatment for triple-negative breast cancer (TNBC), yet toxicity and resistance effects have been the current problems. Curcumin,a natural compound, has been reported to exert anti-proliferative effects on various cancer cells, including breast carcinoma cells. However, the β-diketone moiety influences the stability of curcumin. Curcumin analogs, pentagamavunon-0 (PGV-0), and pentagamavunon-1 (PGV-1) were synthesized to improve the stability and activity of curcumin by modified the β-diketone moiety into mono-ketone pentanone. In this study, we evaluated the cytotoxicity, inhibition of cell cycle progression, and induction of apoptosis of curcumin and its analogs (PGV-0 and PGV-1) in murine triple-negative breast cancer 4T1 cell line. The cytotoxic evaluation was done by MTT assay, while apoptosis induction and cell cycle evaluation was performed by annexin V staining and detected by flow cytometry. Curcumin and its analogs, PGV-0, and  PGV-1, significantly inhibit the viability of 4T1 breast cancer cells with an IC50 value of 34.34µg/mL, 13.76µg/mL and 38.21μg/mL, respectively. Apoptosis analysis with a dose of 10µg/mL and 15µg/mL in 4T1 breast cancer cells showed that curcumin and its analogs effectively induce apoptotic in a dose-dependent manner. In cell cycle analysis using a dose of 15µg/mL, curcumin inhibited the cell cycle progression in the S phase, whereas PGV-0 and PGV-1 inhibited the cell cycle in the G2/M phase. It could be concluded that curcumin analogs, PGV-0 and PGV-1, have higher potential to be developed as anti-cancer agents by inducing cell cycle arrest and apoptosis in triple-negative breast cancer.
Co-Authors . Anindyajati . Larasati Adisusilo, Midori Rahmadhany Putri Aditya Fitriasari Aditya Fitriasari Agusta Fauzi, Ilham Agustina Setiawati Al-Qorin, Fadillah Amaliyatul, Mita Ameilinda Monikawati Andita Pra Darma Angraini, Sonia Meta Anindyajati Anindyajati Anindyajati Anindyajati Arya Nugraha, Reyhan Asep Nuryadin Astrid Ayu Maruti Astrid Ayu Maruti Azmi Rahmadani Bambang Sulistiyo Ari Sudarmanto Bani Adlina Shabrina Cyndwika Ayu Dewi Pratiwi Dewi Pratiwi Dhania Novitasari Dini Maharani Dyaningtyas D. P. Putri Dyaningtyas D.P. Putri Dyaningtyas Dewi Putri Pamungkas Ediati Sasmito Ediati Sasmito Edy Meiyanto Edy Meiyanto Edy Meiyanto Edy Meiyanto Edy Meiyanto Edy Meiyanto Edy Meiyanto Edy Meiyanto Edy Meiyanto Edy Meiyanto Erlina Rivanti Esti, Yuni Fajar Fauziyah Darwis, Rattu Syahada Fazri, Rezi Muhammad Fikri Amalia Guntara, Rangga Gelar Handani, Dewa Ayu Sri Heny Hendrayati Herwandhani Putri Ibrahim Arifin Ika Nurzijah Ikawati, Muthi' Ilham Agusta Fauzi Ilham Augusta F Ilham Augusta F. Indah Hairunisa Indri Kusharyanti Inna Armandari Jenie, Riris Istighfari Juni Ekowati Kartika Dyah Palupi Kartika Dyah Palupi Khairunnisa, Najla Laeli Muntafiah Lailatul Qodria Lailatul Qodria Larasati Larasati Luthfia Indriyani Luthfia Indriyani Maesaroh, Syti Sarah Maran, Gergorius Gena Marcellino Rudyanto Maulid, Zaki Nuraziz Meiyanto, Edy Mokh Adib Sultan, Mokh Adib Muhammad Novrizal Abdi Sahid Musyaffa, Fakhrizal Labib Muthi Ikawati Nanda Resa Pratama Nanda Resa Pratama Naufa Hanif Niken Nur W Niken Nur W, Niken Novi Hastuti Novi Hastuti, Novi Nugraha, Muhammad Rizki Nugraheni, Nadzifa Nur Fitra Sari Nurhaliza, Jelita Nurma Sabila Nurrachma, Marsya Yonna Perdana Adhi Nugroho Pratama, Dimo Purwaamijaya, Btari Mariska Putri, Nindya Budiana Rahmawati, Desty Restia Rahmi Khamsita Rahmi Khamsita Ramadani, Ratna Dwi Ratih Hurriyati Ratna Asmah Susidarti Ratna Asmah Susidarti Ratna Dwi Ramadani Retno Murwanti Ridlo, Muhammad Dzikri Ar Riris Istighfari Jenie Riris Istighfari Jenie Riris Istighfari Jenie Rita Riata Rita Riata Ritmaleni, Ritmaleni Rohmad Yudi Utomo Rosana Anna Ashari, Rosana Anna Rumiyati Rumiyati Sahid, Muhammad Novrizal Abdi Santoso, Christopher Filando Sari Haryanti Sari Haryanti Sarmoko Sarmoko Sendy Junedi Shigeru Sasaki Shigeru Sasaki Sofa Farida Sofa Farida Sukardiman Susi Ari Kristina Susi Ari Kristina Susi Ari Kristina Susi Ari Kristina Tamara, Agra Fadhilla Tutuk Budiati Yanti, Septi Dwi Yullia Febrianti, Sheilla Yurista Gilang Yurista Gilang Zahra, Nasywa